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首页> 外文期刊>Cellular Physiology and Biochemistry >A3 Adenosine Receptor Mediates Apoptosis in 5637 Human Bladder Cancer Cells by Gq Protein/PKC-Dependent AIF Upregulation
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A3 Adenosine Receptor Mediates Apoptosis in 5637 Human Bladder Cancer Cells by Gq Protein/PKC-Dependent AIF Upregulation

机译：A3腺苷受体通过依赖Gq蛋白/ PKC的AIF上调介导5637人膀胱癌细胞的凋亡

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biBackground/Aims /i/bAsub3/sub adenosine receptor mediates apoptosis in a variety of cancer cells via diverse signaling pathways. The present study was conducted to assess Asub3/sub adenosine receptor-mediated apoptosis in human bladder cancer cell lines and to understand the underlying mechanism. biMethods /i/bHuman bladder cancer cell lines such as 253J, 5637, KK-47, TCCSUP, T24, and UMUC-3 cells were cultured. The siRNA to silence the Asub3/sub adenosine receptor-targeted gene was constructed and transfected into cells. MTT assay, TUNEL staining, Western blotting, and real-time RT-PCR were carried out. biResults /i/bFor all the investigated cell types adenosine induced apoptosis in a concentration (0.01-10 mM)- and treatment time (24-48 h)-dependent manner. Adenosine-induced 5637 cell death was significantly inhibited by the Asub3/sub adenosine receptor inhibitor MRS1191 or knocking-down Asub3/sub adenosine receptor, and the Asub3/sub adenosine receptor agonist 2-Cl-IB-MECA mimicked the adenosine effect. The adenosine effect was prevented by GF109203X, an inhibitor of protein kinase C (PKC), but it was not affected by forskolin, an activator of adenylate cyclase. Adenosine-induced 5637 cell death, alternatively, was not inhibited by the pan-caspase inhibitor Z-VAD. Adenosine upregulated expression of apoptosis-inducing factor (AIF), that is suppressed by knocking-down Asub3/sub adenosine receptor, and accumulated AIF in the nucleus. biConclusion /i/bThe results of the present study show that adenosine induces 5637 cell apoptosis by upregulating AIF expression via an Asub3/sub adenosine receptor-mediated Gsubq/sub protein/PKC pathway.
机译：背景/目的 A 3 腺苷受体通过多种信号传导途径介导多种癌细胞的凋亡。本研究旨在评估A 3 腺苷受体介导的人膀胱癌细胞株的凋亡并了解其潜在机制。 方法 培养了253J，5637，KK-47，TCCSUP，T24和UMUC-3细胞等膀胱癌细胞系。构建沉默A 3 腺苷受体靶向基因的siRNA，并将其转染到细胞中。进行了MTT测定，TUNEL染色，蛋白质印迹和实时RT-PCR。 结果 对于所有研究的细胞类型，腺苷以浓度（0.01-10 mM）和治疗时间（24-48 h）依赖性的方式诱导细胞凋亡。 A 3 腺苷受体抑制剂MRS1191或敲低的A 3 腺苷受体和A 3 腺苷受体激动剂2-Cl-IB-MECA模仿了腺苷的作用。腺苷效应被蛋白激酶C（PKC）抑制剂GF109203X阻止，但不受腺苷酸环化酶激活剂forskolin的影响。泛半胱天冬酶抑制剂Z-VAD不能抑制腺苷诱导的5637细胞死亡。腺苷上调凋亡诱导因子（AIF）的表达，该因子可通过敲低A 3 腺苷受体来抑制，并在细胞核中积累AIF。 结论 本研究结果表明，腺苷通过A 3 腺苷受体介导的G q 蛋白/ PKC途径。

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